Synthesis, magnetic properties, biotoxicity and potential mechanism of modified nano zero-valent iron for decolorization of dye wastewater.

SiO2-coated nano zero-valent iron (nZVI) has emerged as a fine material for the treatment of dye wastewater due to its large specific surface area, high surface activity, and strong reducibility. However, the magnetic properties based on which SiO2-coated nZVI (SiO2-nZVI) could effectively separate and recover from treated wastewater, and the biotoxicity analysis of degradation products of the dye wastewater treated by SiO2-nZVI remain unclear. In this study, SiO2-nZVI was synthesized using a modified one-step synthesis method. The SiO2-nZVI nanoparticles were characterized using Transmission electron microscopy, X-ray diffraction, Fourier-transform infrared spectroscopy, Fully automatic specific surface and porosity analyzer, Vibrating sample magnetometer, and Zeta potential analyzer. The removal rate of methyl orange (MO) by SiO2-nZVI composite reached 98.35% when the degradation performance of SiO2-nZVI treating MO was optimized. Since SiO2-nZVI analysed by magnetic hysteresis loops had large saturation magnetization and strong magnetic properties, SiO2-nZVI exhibited excellent ferromagnetic behaviour. The analysis of the degradation products showed that the MO treated by SiO2-nZVI was converted into a series of intermediates, resulting in reducing the toxicity of MO. The potential mechanism of MO degradated by SiO2-nZVI was speculated through degradation process and degradation kinetics analysis. Overall, the SiO2-nZVI composite may be regarded as a promising catalyst for decolorization of dye wastewater.

Correction of DMD in human iPSC-derived cardiomyocytes by base-editing-induced exon skipping.

Duchenne muscular dystrophy (DMD) is caused by mutations in the DMD gene. Previously, we showed that adenine base editing (ABE) can efficiently correct a nonsense point mutation in a DMD mouse model. Here, we explored the feasibility of base-editing-mediated exon skipping as a therapeutic strategy for DMD using cardiomyocytes derived from human induced pluripotent stem cells (hiPSCs). We first generated a DMD hiPSC line with a large deletion spanning exon 48 through 54 (ΔE48-54) using CRISPR-Cas9 gene editing. Dystrophin expression was disrupted in DMD hiPSC-derived cardiomyocytes (iCMs) as examined by RT-PCR, western blot, and immunofluorescence staining. Transfection of ABE and a guide RNA (gRNA) targeting the splice acceptor led to efficient conversion of AG to GG (35.9% ± 5.7%) and enabled exon 55 skipping. Complete AG to GG conversion in a single clone restored dystrophin expression (42.5% ± 11% of wild type [WT]) in DMD iCMs. Moreover, we designed gRNAs to target the splice sites of exons 6, 7, 8, 43, 44, 46, and 53 in the mutational hotspots and demonstrated their efficiency to induce exon skipping in iCMs. These results highlight the great promise of ABE-mediated exon skipping as a promising therapeutic approach for DMD.